Subjects ≥75 years of age are the fastest-growing segment of the population in Western countries. They currently represent 6.0% of the population in the United States and 6.6% in Europe and will become, by the year 2030, >9% and 12%, respectively.1

This age group has the highest risk of cognitive impairment and dementia, and stroke is among the factors that account for this risk.2 Previous studies have found that ≈30% of stroke survivors ≥75 years of age suffer from dementia, a percentage that is considerably higher than in younger stroke patients. In this issue of Stroke, Ballard et al3 present a longitudinal study of a small group of stroke patients ≥75 years of age who underwent a detailed neuropsychological evaluation 3 months after an ischemic stroke and again 1 year later to investigate delayed changes in cognitive functions after stroke and to verify whether commonly used criteria for early cognitive impairment, ie, mild cognitive impairment, aging-associated cognitive decline, and vascular cognitive impairment, no dementia (vascular CIND), were able to predict cognitive deterioration. The proportion of patients experiencing a decline in cognitive functions was 30%, with 9% developing dementia. However, cognitive improvement was observed in ≈50% of the patients, and 16% showed an increase of >2 points in the Mini Mental State Examination score. This study adds to the previous literature because it demonstrates that none of the proposed criteria for identifying subjects with cognitive impairment at high risk for dementia, including vascular CIND, can predict which stroke patients will develop dementia. This finding, which needs to be replicated in other samples, confirms the existence of an important knowledge gap in this area: the criteria for cognitive impairment in stroke patients need to be refined considering the peculiar characteristics of this population.4 Identification of the patients who have a high probability of experiencing cognitive decline and developing dementia after stroke would be of paramount importance in planning intervention trials aimed at preventing these dreadful outcomes, but this is not going to be an easy task. First, cognitive changes after stroke have a highly dynamic course in the months after the acute event, as confirmed by the study of Ballard et al. Moreover, poststroke dementia patients are a heterogeneous group, not only because of the different features of the stroke but also because a considerable percentage has preexisting cognitive impairment.5 In view of the complexity of the mechanisms likely to be responsible for poststroke dementia, several other factors besides neuropsychological performance should be taken into account. Sociodemographic factors (eg, older age, low education attainment), prestroke cognitive impairment, stroke features (severity, location, recurrence), neuroradiological features (extent of white matter lesions, medial temporal lobe atrophy), and comorbidities (eg, diabetes mellitus, diseases inducing hypoxia or ischemia such as myocardial infarction, atrial fibrillation, and pneumonia) have been associated in some studies with a higher probability of dementia after stroke.5–7 Longitudinal studies are needed with serial assessment of clinical, neuroradiological, neuropsychological, and possibly biological data, starting immediately after the ischemic stroke. This study design would allow detection of the occurrence of delirium, a condition that might be a marker, even in subjects without preexisting cognitive impairment, of an increased risk of dementia,8 and evaluation of the long-term effects of acute management of ischemic stroke on cognitive functions.